Human health implications of A1 versus A2 beta-casein: theory and current evidence

[On March 21 2014 I presented a paper at a conference organised by UK charity Food and Behaviour Research and held at the Royal College of Surgeons, London. The abstract is copied below]

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Human Health Implications of A1 versus A2 beta-casein: theory and current evidence

Keith Woodford
Professor of Farm Management and Agribusiness
Lincoln University, New Zealand

The health implications of A1 beta–casein relative to A2 beta-casein are controversial. At times the scientific debate can become clouded by the reality that milk is a commercial product. Conversion of all herds so as to replace A1 beta-casein with A2 beta-casein over one to two cow generations (4 – 12 years) is technically straight forward. Accordingly, the beta-casein issue can be presented as either a threat to, or an opportunity for, the mainstream industry, with elements of each perspective being valid.

The Key Science.

  • All bovine beta-casein was originally of the A2 type. A1 beta-casein is now produced by a considerable proportion of cows that have European bloodlines. In contrast, goats, sheep, buffalo, camels and humans produce beta-casein of the A2 type.
  • On digestion, A1 beta-casein releases the peptide beta-casomorphin-7 (BCM7) which has opioid characteristics. This is scientifically proven and is no longer controversial. The level of release has been shown to be consistent with pharmacological effects (Boutrou et al 2013)
  • A1 beta-casein has been implicated in a range of human health conditions, many of which have an auto-immune element to them. The health conditions include Type 1 diabetes, heart disease, mental health conditions, behaviour, child development, sudden infant death syndrome, and milk intolerances.
  • The evidence in humans is largely epidemiological (population studies, cohort studies, case-control) and observational, plus in vitro for human tissues, and randomised trials with animals.
  • New research with rats (Barnett et al 2014) has shown, with major and statistically significant effect sizes, that A1 beta-casein inhibits gastric transit of food relative to A2 beta casein, that the enzyme DPP4 is up-regulated in the small intestine, and that in the colon there is an increase in the inflammatory marker myeloperoxidase (MPO).
  • A recent study with mice (Haq et al 2013) found that in response to A1 beta-casein ingestion there were major effects (both size and statistical significance) in immune responses (antibodies and Th2 cell production) and intestinal myeloperoxidase (MPO). These effects did not occur with A2 beta-casein.
  • This recent research can help provide theoretical underpinnings for the prior epidemiological findings and further justify the revisiting thereof.
  • It is feasible for all dairy herds to be bred to remove the A1 allele relating to the specific gene that produces A1 beta-casein. Total herd conversion can take anywhere from four years to about twelve years, depending on the breeding strategy.

Recent references
Barnett MPG, McNabb WC, Roy NC, Woodford KB, and Clarke AJ 2014. “Dietary A1 beta-casein affects gastrointestinal transit time, dipeptidyl peptidase-4 activity, and inflammatory status relative to A2 b-casein in Wistar rats”. International Journal of Food Sciences and Nutrition. In press.

Boutrou R, Gaudichon C, Dupont D, Jardin J, Airinei G, Marsset-Baglieri A, et al. Sequential release of milk protein-derived bioactive peptides in the jejunum in healthy humans. American Journal of Clinical Nutrition. 2013;97(6):1314-23. Epub 2013/04/12.

Haq MR, Kapila R, Sharma R, Saliganta V, Kapila S. 2013 “Comparative evaluation of cow β-casein variants (A1/A2) consumption on Th2-mediated inflammatory response in mouse gut”. European Journal of Nutrition. Epub 2013/10/10.

Further Information:
Keith Woodford writes extensively on the topic of A1 versus beta-casein. His archived writings including detailed references on this topic can be found at http: //keithwoodford.wordpress.com within the website category ‘A1 and A2 milk’.

Disclosure of Interest
On occasions Keith Woodford consults in a professional capacity for A2 Corporation and other agri-food companies as an independent adviser. However he does not represent any   of these companies and he retains total independence in anything that he writes.

About Keith Woodford
Keith has been Professor of Farm Management and Agribusiness at Lincoln University, New Zealand, since 2000. His professional interests span from farm decisions though to food and health outcomes. This current semester he is teaching into a new Lincoln University course in global food systems. He has supervised 12 PhD students and more than 20 Masters students through to completion. Previously he was Reader in Rural Management at University of Queensland in Australia. He has worked on agri-food projects in many Asian and Pacific countries, working for national and international development agencies and also commercial firms. He has been studying and writing on the science and politics of A1 and A2 beta-casein for more than 10 years. His book ‘Devil in the Milk.’ was published in 2007, with an updated version in 2010. Outside of agri-food systems, his lifelong passions include mountaineering and skiing.

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About Keith Woodford

Keith Woodford is an independent consultant, based in New Zealand, who works internationally on agri-food systems and rural development projects. He holds honorary positions as Professor of Agri-Food Systems at Lincoln University, New Zealand, and as Senior Research Fellow at the Contemporary China Research Centre at Victoria University, Wellington.
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15 Responses to Human health implications of A1 versus A2 beta-casein: theory and current evidence

  1. Pingback: Rural round-up | Homepaddock

  2. GrassFood says:

    I just finished your book, The Devil in the Milk, and so appreciate your work. I have three family Jersey cows and tested them (UC Davis) and two came back A1/A2. 😦 We love them very much and I read that the “milk devil” does digest out in yogurt and cheese and I assume kefir, but I am curious if it would be removed in making butter, or ghee? Thank you very much.

  3. Pingback: A Short History of Milk: A1 vs. A2 - A Worthey Read!

  4. Ken Flye says:

    I am just finishing your book “Devil…” and am flaggergasted. It seems we have to go through the same rigamarole with each new discovery concerning the dangers of the food industrial complex. Thank you so much for your courageous truth telling. I am a water aerobics instructor in Portland,Oregon USA and have been trying to spread the word about this and issues related to sugar and grain consumption as well. All the best, Ken Flye

  5. Min Giffard says:

    I’ve just finished reading ‘Devil in the Milk’ and subsequently have popped onto your website to see what the latest instalments were on the topic. My partner can verify that I’ve been talking non stop about this book the last 2 weeks whilst reading it. The quantity of evidence supporting the A2 story is quite remarkable and in my view compelling. I work as a GP and am thinking of the number of patients I’ve come across over the years who may benefit from switching to A2 milk. We had started buying A2 milk only just before starting to read your book based on the fact that my partner thinks it tastes better and he feels his sinus issues are less troublesome on A2 milk. We will not be switching back. I’m currently pregnant and since it is so easy to access A2 products, I don’t see the point in purchasing regular milk when the implications are potentially as substantial as the research is suggesting. Not only did I appreciate the information you presented on a purely intellectual and professional basis, but I thoroughly enjoyed seeing how the whole A2 topic unfolded and continues to unfold from a storytelling manner. Thank you.

  6. Manju says:

    It’s a matter of great concern. Consumers
    should be made aware of there facts.

  7. rita sunderland says:

    I am unable to find a store that carries the a2 milk, i desperately need to start consuming this product

  8. Mel says:

    Hi I am currently looking into the A2 milk scenario again for a paper i’m writing. Am re reading your book and wondering about the significance of Vitamin D and Type 1 Diabetes as one of the risk factors. Have you covered this in any later articles? Or know if it has been explored with the milk issue? I know you talk about it in the book mainly in relation to MS and have found some moderate quality research that seems to be highly regarded at times but please let me know if you know any more.

    Cheers
    Mel.

    • Mel says:

      ….especially any A1 milk studies controlling for Vitamin D exposure or vice versa.
      Thanks!

      • Keith Woodford says:

        Mel
        This is a quick response to a big topic.
        The arguments for VitD as a major causal or mediating factor in relation to Type 1 diabetes have largely fallen away in the last few years. But that does not mean that it is not relevant. It could still be a mediating effect, but there is no evidence for it being the major causal effect. It certainly cannot explain the population epidemiology of Type 1 diabetes.
        Keith

      • mel says:

        HI thanks for reply, yes i was thinking so, due to the Iceland phenomenon at least. Let me know if there are any recent studies in relation to Type 1 diabetes especially in humans. I’ll look up the peptide one above. Who funds the research into these studies? The hydrolyzed casein studies seem to be very extensive/expensive and i gather are funded through the respective manufacturing industries. A big question again!

  9. Keith Woodford says:

    Mel
    There are hundreds of recent studies on diabetes but there are no earth shattering results. That is what happens when people keep asking the wrong research questions.
    I am part of a team that has been reviewing the evidence for A1 beta-casein as the prime causal agent, but that study is only in the early stages of peer review. As to how long that peer review process will take, and the length of the winding path through to publication, I would only be guessing.
    As a general comment it is very hard to prove the cause of diseases that take so long to manifest themselves.
    Keith W

    • mel says:

      Yes i was meaning T1D studies regarding the A1 beta-casein as a risk factor/causation. This new review sounds good, will look forward to reading it. Yes there are many causative factors with chronic disease as there are many ways we have slowly (but too quickly in evolutionary terms) changed the lifestyle for which humans have evolved. Hopefully it can slowly be changed back…. Selective breeding activities for yield and protein content must have seemed like a great idea at the times that they were instituted….to get more food faster etc or to build economies but not great regarding health effects to meddle with natural processes and probably not the best for animals either. Would be interesting to look at infant digestion in calves re A1/BCM7 vs A2!?? Long term studies for chronic disease are probably not a priority however since cattle don’t usually ‘live til they die’ in a commercial situation.

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